phys-cardiovascular notes 2
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phys-cardiovascular notes 2

Course Number: PHYS 100, Fall 2010

College/University: Saint Louis

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Electrical Activity of the Heart -the pacemaker= SA node begins AP -conduction of the system of the heart -spread of excitation through the heart muscle -ionic basis of electrical activity in the heart -electrical activity in cardiac contractile cells -recording the electrical activity of the heart with an electrocardiogram How does pacemaker work? Autorhythmic cells- ability to generate own rhythm Sinoatrial node...

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Activity Electrical of the Heart -the pacemaker= SA node begins AP -conduction of the system of the heart -spread of excitation through the heart muscle -ionic basis of electrical activity in the heart -electrical activity in cardiac contractile cells -recording the electrical activity of the heart with an electrocardiogram How does pacemaker work? Autorhythmic cells- ability to generate own rhythm Sinoatrial node (SA node) 1. generates the rhythm 2. heart's pacemaker Conductile System 1. pace maker cells -spontaneously depolarizing membrane potentials to generate action potentials 2. conduction fibers - rapidly conduct action potentials initiated by pacemaker cells to myocardium -conduction velocity= fast (4m/s) -skeletal muscle fibers= slower than cardiac conduction fibers (.4 m/s) Pacemaker cells of myocardium 1. pacemaker cells -SA node (pacemaker of the heart, set the rhythm) -AV node *then go into ventricle to.... 2. conduction fibers -internodal pathways -bundle of His -Purkinje fibers (main contraction) Autorhythmic Cells Location Firing Rate at Rest SA Node (sets rhythm) 70-80 APs/min* AV Node 40-60 APs/min (not optimal, but not death) Bundle of His 20-40 APs/min Purkinje Fibers 20-40 APs/min Fastest depolarizing cells control other cells Fastest cells = pacemaker - set rate for rest of heart * action potentials per minute (tonic control by parasympathetic nervous system) otherwise ~ 100 APs/min -parasympathetic has a large impact *if SA node not working, alternative cells activate: it is not optimal, but it allows you not to die *ion movement across gap junctions is the electrical current in the heart both atria contract at the same time AV node contracts slower so that all the blood can leave the atria Spread of Excitation 1. Interatrial pathway -SA Node (pacemaker) -Rapid Conduction -simultaneous contraction of right and left atria -atria contacts before the ventricles 2. Internodal pathway SA Node--> AV Node (AV node delay= .1 s) *delay because blood must be emptied from atrias 3. AV Node transmission -ONLY pathway from atria to ventricles -slow conduction 4. Ventricular excitation -DOWN bundles of His (fast: 2m/s) -UP Purkinje fibers (even faster: 4m/s) -Purkinje fibers contact ventricle contractile cells -Ventricle contracts from apex up *picture Electrical Activity: 2 different action potentials 1. Pacemaker cell action potential -SA node 2. Contractile cell must accept action potential -cardiomyocyte (contraction depends on the ion movement= electrical activity) Pacemaker Cell: 1) spontaneous depolarization funny channel opens Na in K out 2) spontaneous depolarization *ion leakage= change in membrane potential T-type Ca channel opens Ca in *where beat of the heart is 3) rapid depolarization phase L-type calcium channels open Ca in *large Ca channel because a lot of Ca comes in 4) repolarization phase of action K channels open K out -has phase 0 (rapid depolarization), 3 (repolarization), 4 (resting potential) Contractile Cell Action Potential: 5 phases -Phase 0: increased Na conductance (IN) - Phase 1: decreased Na conductance & transiet K conductance (OUT) - Phase 2: increased Ca conductance (IN) - Phase 3: increased K conductance (OUT) -Phase 4: resting membrane potential *long duration of action potential = 250-300 m/sec (only 1-2 m/ sec in skeletal) 0: rapid depolarization 1: small repolarization 2: plateau 3: repolarization 4: resting potential Electrical Activity of the Heart -can be recorded from electrodes on the skin -non-invasive technique (paste on electrodes) -used to test for clinical abnormalities regarding conduction of electrical signals in the heart Electrocardiogram= external measure of electrical activity of the heart -body= conduction -currents in body can spread to surface (ECG, EMG, EEG) -distance and amplitude of spread depends on size of potentials and synchronicity of potentials -heart electrical activity- synchronized because of intercalated disks Einthoven's Triangle Lead I: Left Arm (+) and Right Arm (-) Lead II: Left Leg (+) and Right Arm (-) Lead III: Left Leg (+) and Left Arm (-) Electrical Activity of Heart P wave: atrial depolarization QRS wave: ventricular depolarization and atrial repolarization T wave: ventricular repolarization PQ segment: AV nodal QT segment: ventricular systole TP ventricular interval: diastole ECG Arrhythmias: Abnormal rates -sinus rhythm: pace generated by SA node -modified by parasympathetic (slow- bradycardia) and sympathetic (fast-tachycardia) nervous system input -abnormal rates shown 1. tachycardia= fast rhythm 2. bradycardia= slow rhythm ECG Arrhythmias: Fibrillation -Ventricular Fibrillation 1. loss of coordination of electrical activity of heart 2. death can ensue within minutes unless corrected Cardiac Output and its control 1. autonomic input to the heart -sympathetic (increase) -parasympathetic (decrease) 2. factors affecting cardiac output -changes in heart rate (HR) -changes in stroke volume (SV) *how much blood we eject during heart beat Cardiac Output= volume of blood pumped by each ventricle per minute -Cardiac output (CO) = SV x HR - Average CO= 5 L/min at rest -Average (whole body) blood volume: 5.5 L Regulation of Cardiac Output= regulation of heart rate and stroke volume -ANS -Hormonal (epinephrine/norepinephrine) -Autoregulation Autonomic inputs to heart 1. parasympathetic fibers go to SA node and AV node 2. sympathetic fibers go to SA and AV nodes AND ventricular myocardium Heart Rate- Determined by SA node firing rate -SA node intrinsic firing rate= 100/ min *with no extrinsic control on heart -SA node under control of ANS and hormones (extrinsic control) *rest: parasympathetic dominates (HR: 75) *excitement: sympathetic takes over (HR increases up to 150+) Effects of Sympathetic Activity on Heart Rate Increased sympathetic or hormonal activity --> (ANS or epinephrine from adrenal gland) --> Beta 1 adrenergic receptors in SA node --> Increase open state of Na+ and Ca2+ channels --> more ions come in= more AP Increase rate of spontaneous depolarization --> Increase heart rate **SYMPATHETIC EFFECTS SA CELLS *allow more ions to move in and a quicker depolarization -T-type channels are all or none? Effects of Parasympathetic Activity on heart rate Increased parasympathetic activity (vagus nerve) --> Muscarinic Cholinergic Receptors in SA Node --> Increase open state of K+ channels and closed state of Ca channels --> Decrease rate of spontaneous depolarization and hyperpolarize cell --> Decrease heart rate norephinephron-muscarinic receptor- G protein- deactivate of Ca channel- open K channel (K can leave) Regulation of Cardiac Rate -Norepinephrine and epinephrine stimulate opening of pacemaker Na & Ca Channels *this depolarizes SA node faster= increases heart rate -ACh promotes opening of K channels *the K outflow slows depolarization= decreases heart rate AV Nodal Innervation 1) Sympathetic -increases conduction velocity through node -increase HR *epinephrine from the adrenal gland works like norepinephrine from sympathetic 2) Parasympathetic -decreases conduction velocity through node -decreases HR Factors Affecting Cardiac Output: Stroke Volume *primary factors affecting stroke volume: 1. ventricular contractility (contractile force) 2. end-diastolic volume-preload 3. afterload (pressure after contraction) Extrinsic Control of Stroke Volume -Sympathetic innervation of contractile cells -increases cardiac contractility -Parasympathetic innervation of contractile cells -not important -hormones -thyroid hormones (insulin and glucagon) increase force of contraction Sympathetic Effects on Contractility -increased sympathetic activity -increases strength of contraction -increases rate of contraction -increase relaxation of contraction Principle of Frank-Starling's Law -increase LEDV stretches muscle -optimum length= greater strength of contraction -result= increased SV Intrinsic Control: Frank-Starling's Law Increase venous return (Preload) --> Increase strength of contraction-->Increase stroke volume (SV) ex: increase in venous return::Lay down= different blood flow Factors Affecting End-Diastolic Volume -End diastolic pressure= preload -filling time -atrial pressure -central venous pressure -Afterload= pressure in aorta during ejection Lymphatic System -transports intersitial fluid (lymph) back to blood Lymphatic capillaries= closed end tubes that collect interstitial fluid from tissues -very porous Lymph is carried from lymph capillaries to: 1. lymph nodes where lymph is filtered 2. then to lymph ducts where lymph is returned to the blood

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